Outer hair cells are similar to inner hair cells in that they convert sound-induced mechanical vibration into electrical signal as the mechano-sensory cells in the ear. However, outer hair cells also work reciprocally, acting as a fast motor capable of amplifying the mechanical vibration to which these cells respond. These properties of outer hair cells are responsible for the sensitivity and the sharp frequency discrimination of the mammalian ear. We have previously established that the hair cell motor uses electrical energy available at the plasma membrane in a manner similar to piezoelectricity, based on the coupling of electric charge transfer across the membrane with membrane area changes. Specifically, this motility can be reasonably explained by a simple two state model in which two states differ in charge and membrane area but not in the mechanical compliance. The area difference is determined by tension dependence of the motor activity.[unreadable] [unreadable] This model leads to a biphasic dependence of the axial stiffness analogous of gating compliance. However, experimentally observed axial compliance monotonically increases with depolarization. This observation may appear explainable by assuming that a large compliance of the motor state with smaller membrane area. Such an assumption, however, leads to incorrect tension dependence of the motor. It is found that this inconsistency is associated with the condition that increased membrane tension reverses the size of membrane areas of the two states. To avoid this inconsistency, the compliance of the state with smaller membrane area must decrease rapidly as membrane tension increases. That means that the axial compliance that is monotonic with respect to voltage can be predicted only if turgor pressure is less than 0.1 kPa, somewhat less than reported estimates.[unreadable] [unreadable] To understand molecular details of the membrane motor, we examined effects of a sets of chemicals. GsMTx4, a cationic hydrophobic peptide isolated from tarantula venom, is a specific inhibitor of stretch-activated channels. We showed that the toxin also affects the membrane motor of outer hair cells at low doses. The toxin shifts the operating point of the motor up to 25 mV, capable of significantly reducing the performance of the ear. The dissociation constant is about 5 fold higher than that for stretch activated channels. Our analysis indicates that the interface of the motor molecule with lipid bilayer is the likely site of action.[unreadable] [unreadable] To test a hypothesis that there are factors that help the function of the membrane motor, we examined ionic currents in outer hair cells. We found that basal turn outer hair cells in guinea pigs, which operate at high frequency, have a fast ion current that activates less than 0.3 ms at room temperature, and that such currents were absent in apical turn cells, which operate at lower frequencies. This finding is consistent with our previous theoretical analysis that a fast-activating potassium current is required only in the basal turn to counteract the capacitive current and thereby to enhance the voltage oscillation that drives the motor. Thus our finding is consistent with the functional significance of electrically driven motility. We conjecture therefore that the current that we observed reduces the capacitance of the outer hair cell so that the cells' motile activity is effective at high frequencies.